Release of 3H-5-hydroxytryptamine by amiflamine and related phenylalkylamines from rat occipital cortex slices

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Abstract
In the present study Amflamine and other related reversible monoamine oxidase-A (MAO-A) inhibitory phenylalkylamines were examined in vitro for their ability to induce release of 3H-5-hydroxytryptamine (3H-5-HT) from rat occipital cortex slices. The slices were preincubated with 3H-5-HT 0.1 μmol/l in the presence of the irreversible MAO inhibitor pargyline 50 μmol/l and then continuously superfused. The effects were compared with those of the 5-HT releaser p-chloroamphetamine (pCA), the reversible MAO-inhibitor α-ethyltryptamine and the 5-HT uptake inhibitor citalopram. Amiflamine, some related compounds and α-ethyltryptamine which in vivo after transport by the 5-HT uptake mechanism preferentially inhibit MAO within the serotonergic neurons caused a Cat2+-independent release of 3H-5-HT. Some transported compounds, particularly NBF 027 were, however, very weak releasers of 5-HT. This release and that induced by pCA was prevented by citalopram in the superfusion medium. FLA 365, FLA 417 and FLA 1088, which are not transported into the neurons, were poor releasers of 5-HT. It is concluded that compounds which were effective releasers of 5-HT in vitro were those that are transported into the serotonergic neurons by the 5-HT carrier in vivo and has in addition an ability to mobilise vesicular 5-HT.

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